The Gα protein FveGPA1 regulates inflorescence architecture via the FveBRI1-mediated brassinosteroid pathway in strawberry

Inflorescence architecture determines fruit number and size, making it a critical agricultural trait. In strawberry, inflorescences display distinct branching patterns that correlate with fruit size uniformity, but the underlying genetic mechanisms remain poorly understood. Here, we identified four basal-branching inflorescence mutants (bbi1-1, bbi1-2, bbi2-1, and bbi2-2) in woodland strawberry (Fragaria vesca), whose inflorescences are partially basal-branching compared to the upper-branching inflorescences of the wild type. The heterotrimeric G-protein α-subunit gene FveGPA1 is responsible for the defects in bbi1-1 and bbi1-2, whose phenotypes are further enhanced by a mutation in the γ-subunit gene FveAGG3. The brassinosteroid (BR) receptor gene FveBRI1 is the causal gene for the bbi2-1 and bbi2-2 mutants. Notably, bbi1 bbi2 double mutants produce exclusively basal-branching inflorescences, a more severe phenotype than single mutants, suggesting a synergistic interaction between FveGPA1 and FveBRI1. Gene expression analysis, BR sensitivity assays, and BR metabolite quantification, together with the observed rescue of the bbi1 phenotype through loss-of-function of the BR metabolic enzyme CYP734A129, collectively indicate that FveGPA1 regulates inflorescence architecture via the BR signaling pathway. This phenotypic change is driven by differential elongation of the peduncle and pedicel due to cell division and expansion. Our findings reveal a molecular framework for inflorescence internode elongation mediated by the heterotrimeric G-protein and BR pathways and provide a theoretical basis for optimizing strawberry inflorescence architecture.